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Biomedical subjects

E Thaulow

Publications and source records attributed to E Thaulow.

14 recordsLinked to original sources
PubMed1992

[Glyceryl trinitrate patches during continuous intravenous infusions].

A randomized, double blind comparison of the incidence of removal of patches because of venous occlusion was performed in patients on continuous intravenous fluid therapy using 2.5 mg trinitroglycerine or placebo patches attached to the thorax. The sample comprised 90 patients, of whom nine were excluded for administrative reasons. Of the remaining 81,41 received active and 40 received placebo patches. Within one week 11 venflones occluded; ten in patients on placebo, and one in a patient with an active trinitroglycerine patch. Finally 14 (11 placebo and three trinitroglycerine) patches occluded. This tendency in favour of trinitroglycerine patches was statistically significant (p = 0.018). No difference in frequency of thrombophlebitis was observed: (14 versus 18 not leading to occlusion). Seven patients on trinitroglycerine and one on placebo developed moderate headache which did not necessitate withdrawal of treatment. It is concluded that 2.5 mg trinitroglycerine patches seem to improve survival of venflones used for continuous, intravenous fluid therapy, even when applied to the thorax.

Administration, Cutaneous↗
PubMed1992

Haemodynamic and neurohumoral effects of cold pressor test in severe heart failure.

The effect of a cold pressor test (CPT) on haemodynamics in relation to general and regional sympathetic activity and arginin vasopressin (AVP), was studied in eleven patients with severe congestive heart failure (CHF). Compared to an age-matched control group (C), resting arterial plasma noradrenaline (NA) (419 +/- 77 vs. 182 +/- 15 pg ml-1), and adrenaline (A) (142 +/- 28 vs 54 +/- 10 pg ml-1) were higher (P less than 0.05) in CHF. AVP showed no significant difference (14 +/- 4 vs. 9 +/- 4 pg ml-1). During CPT systolic and diastolic blood pressure and systemic vascular resistance increased (P less than 0.01), as did NA (delta 114 +/- 39 pg ml-1, P less than 0.01), A (delta 33 +/- 10 pg ml-1, P less than 0.01) and heart rate (delta 10 beats min-1, P less than 0.01). The myocardial v-a difference of NA decreased (P less than 0.05), but was unchanged across the renal vascular bed during CPT. The a-v difference of NA in the hepatic vascular bed, and fractional extraction of A in the coronary sinus, renal and hepatic vascular beds remained unchanged during CPT. AVP did not change significantly and no change in cardiac index or left ventricular filling pressure was observed during CPT. These data suggest that despite an increased activation of the sympathetic nervous system at rest, a further increase in blood pressure and catecholamines took place during CPT. Thus, the effect of a CPT which activates the central sympathetic system seems not to be altered in patients with severe CHF.

Aged↗
PubMed1991

[Stiffness of the heart--stunning].

The article describes "stunning", or "myocardial post-ischemic dysfunction". An animal model is presented to introduce the characteristics of the phenomenon, and data from a clinical trial are referred in order to demonstrate the clinical relevance of stunning. The long-standing lethargy experienced by many patients with coronary artery disease several hours after exercise may be caused by stunning. It is necessary to know the phenomenon in order to realize why myocardial contractility may be temporarily reduced, not only during but also after ischemic episodes.

Animals↗
PubMed1991

[Prolonged action nitrates in stable angina pectoris].

A randomized double blind comparison of transdermal nitroglycerin and isosorbide dinitrate tablets was conducted in 100 men with stable angina pectoris. Subjective and objective effects were virtually identical for both regimens (number of angina attacks/nitroglycerin consumption and exercise ECG test variables). The pattern of side effects was also similar for both drugs. A considerable dissociation was observed between subjective effects and effects measured by ergometer test in the individual patient. Lack of both subjective and objective effects--i.e. nitrate tolerance--was observed in approximately one fourth of the patients, and was not prevented by a twelve-hour dosing interval on isosorbide dinitrate nor a six hour transdermal nitroglycerin-free interval. Our data lends credence to the notion that the effects of long-acting nitrates in daily life and the effects measured during stress testing may involve different mechanisms.

Administration, Cutaneous↗
PubMed1991

Interventricular redistribution of myocardial blood flow during metabolic vasodilation.

To determine the effect of metabolic vasodilation on the blood flow distribution within the hypoperfused left anterior descending coronary artery (LAD) of the pig (a perfusion bed containing both left and right ventricular myocardium), 28 anesthetized (isoflurane) pigs were studied during intracoronary dobutamine infusion (2.5 +/- 1, SD, micrograms/min) at two levels of reduced, constant coronary inflow. In 8 pigs, coronary inflow was reduced from 59 +/- 9 ml/min to 42 +/- 10 ml/min; coronary perfusion pressure fell to 62 +/- 2 mm Hg (8260 +/- 260 Pa) and then fell further to 54 +/- 6 mm Hg (7190 +/- 800 Pa) during dobutamine infusion. Subendocardial blood flow in the anterior wall of the left ventricle perfused by the LAD decreased from 0.64 +/- 0.12 ml min-1 g-1 with hypoperfusion alone, to 0.40 +/- 0.14 ml min-1 g-1 (P less than 0.002) with the addition of dobutamine. Conversely, blood flow to the right ventricular region supplied by the LAD increased significantly from 0.78 +/- 0.40 ml min-1 g-1 (hypoperfusion alone) to 0.92 +/- 0.50 ml min-1 g-1 (P less than 0.008) with dobutamine. In 10 pigs, a more severe reduction of coronary inflow to 26 +/- 12 ml/min and subsequent dobutamine infusion resulted in a similar redistribution of blood flow from the left to the right ventricular portion of the perfusion bed. Infusion of dobutamine during hypoperfusion, but with a pressure-constant perfusion system, was associated with increases in blood flow to both the right and left ventricular portions of the perfusion territory.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

How important is heart rate?

Mortality rises as resting heart rate increases. Patients who are less able to increase their heart rate while exercising are more likely to die than those whose heart rate does rise. The occurrence of silent ischaemic events shows a circadian distribution, with increased mortality, heart rate and systolic blood pressure early in the morning. Treatment with beta-blockers reduces the number of asymptomatic ischaemic episodes, and lowers heart rate during exercise and at rest. The ischaemic myocardium of the dog loses the ability to undergo wall thickening during exercise. Moreover, blood flow in the ischaemic subendocardium is reduced during exercise. These effects can be overcome using beta-blockers. The effects of beta-blockers in reducing heart rate are less pronounced during mental stress. Furthermore, changes in wall motion abnormalities during mental stress are not improved by beta-blockers. Treatment of patients with beta-blockers after a myocardial infarction reduces the mortality rate. The greater the reduction in heart rate, the greater the reduction in mortality.

Adrenergic beta-Antagonists↗
PubMed1991

Blood platelet count and function are related to total and cardiovascular death in apparently healthy men.

BACKGROUND: Experimental animal and clinical studies indicate that blood platelets have an important role in atherosclerosis and formation of thrombi. Prospective studies presenting evidence of an association between blood platelet count and cardiovascular mortality have not been performed. METHODS AND RESULTS: From 1973 to 1975, blood platelets were counted, and their responsiveness to aggregating agents was studied in healthy middle-aged men. The aim was to assess the possible association between these variables and coronary heart disease. At 13.5 years of follow up, a significantly higher coronary heart disease mortality was observed among the 25% of subjects with the highest platelet counts. Platelet aggregation performed in a random subsample (150 of the 487 men), moreover, revealed that the 50% with the most rapid aggregation response after ADP stimulation had significantly increased coronary heart disease mortality compared with the others. These associations could not be explained by differences in age, lipids, blood pressure, or smoking habits. CONCLUSIONS: The present study is the first to present conclusive, prospective evidence of an association between platelet concentration and aggregability and long-term incidence of fatal coronary heart disease in a population of apparently healthy middle-aged men.

Adenosine Diphosphate↗
PubMed1990

Alpha-adrenergic regulation of myocardial performance in the exercising dog: evidence for both presynaptic alpha 1- and alpha 2-adrenoceptors.

New evidence supporting both presynaptic alpha 1- and alpha 2-adrenoceptors playing a role in the regulation of myocardial contractile performance in the exercising dog is reviewed. Studies utilized chronically instrumented dogs having sonomicrometers for the measurement of regional wall thickening and transducers for the measurement of left ventricular and systemic hemodynamics. During steady state exercise, either the selective alpha 1-adrenoceptor blocker prazosin (80 micrograms/kg) or the selective alpha 2-adrenoceptor blocker idazoxan (80 micrograms/kg) was infused into the left atrium while exercise continued. Immediately following the administration of either alpha-adrenoceptor blocking agent, there were substantial increases in heart rate, left ventricular dP/dt and regional contractile function as assessed using sonomicrometers, and norepinephrine release by the myocardium increased substantially. beta-adrenergic blockade prevented the heart rate and contractile effects of either alpha 1- or alpha 2-adrenoceptor blocker whereas norepinephrine release was further enhanced. These effects could not be attributed to baroreceptor unloading. In dogs studied under resting conditions with norepinephrine infusion to produce an increase in dP/dt similar to that observed during treadmill exercise, no sympathetic augmentation was observed following either alpha-blocker. Together, these studies provide evidence that both alpha 1- and alpha 2-adrenoceptors participate in the modulation of sympathetic neuronal norepinephrine release in the canine myocardium.

Adrenergic alpha-Antagonists↗
PubMed1990

Myocardial effects of selective alpha-adrenoceptor blockade during exercise in dogs.

To study the effect of selective alpha 1- or alpha 2-adrenergic blockade on the myocardial contractile and chronotropic response to exercise, 29 dogs were chronically instrumented with a sonomicrometer for measuring myocardial wall thickness and a micromanometer for measuring left ventricular pressure. During treadmill exercise, either the selective alpha 1-blocker prazosin (80 micrograms/kg, n = 12) or the alpha 2-blocker idazoxan (80 micrograms/kg, n = 8) was infused into the left atrium beginning 2-3 minutes after the onset of exercise. alpha 1-Adrenoceptor blockade, like alpha 2-adrenoceptor blockade, was found to cause significant increases in systolic wall thickening, thickening velocity, heart rate, and left ventricular contractility, indicating an increase in inotropic state that was comparable to that with alpha 2-adrenoceptor blockade. Preventing the decrease in aortic blood pressure after selective alpha 1-blockade by using either systemic angiotensin II infusion (n = 6) or inflation of an intra-aortic balloon (n = 6) did not prevent the observed increases in wall thickening, heart rate, and left ventricular contractility. In four of the dogs treated with prazosin, the norepinephrine concentration in the coronary sinus was found to more than double after alpha 1-blockade. beta-Adrenergic blockade (propranolol, 1.0 mg/kg) prevented the increased contractile and chronotropic state caused by alpha 1- or alpha 2-blockade. Selective alpha-adrenergic blockade during adrenergic activation by intravenous norepinephrine infusion, in contrast to exercise, had no effect on wall thickening, heart rate, or left ventricular contractility. These data indicate that selective alpha 1-adrenergic blockade, like selective alpha 2-adrenergic blockade, causes a significant augmentation of heart rate and left ventricular contractility in the dog during dynamic exercise. These data are consistent with the hypothesis that this occurs through a presynaptic disinhibition of neural norepinephrine release mediated by a prejunctional alpha 1-adrenoceptor.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Electrophysiological and hemodynamic disturbances in a patients overdosed with disopyramide.

Disopyramide exerts a quinidinelike effect on the heart and is a valuable drug for treating atrial and, especially, ventricular tachyarrhythmias. The therapeutic plasma concentration of disopyramide is thought to be 2.0-4.0 (5.0) microgram/ml. We here report the cardiac effects of a high dose of disopryamide in a patient with extensive coronary artery disease complicated by ventricular extrasystoles. At plasma levels above approximately 7.0 micrograms/ml, heart rate was decreased, while PQ interval, width, and QT interval were increased. At concentrations above approximately 6.0 micrograms/ml, disopyramide exerted negative intropic effects as judged by increases in mean right atrial, pulmonary arteriolar, and pulmonary capillary venous pressures and a decrease in cardiac output.

Adult↗